Obstructive sleep apnoea (OSA) is due to craniofacial changes and acromegal
y. The question addressed by this study was whether growth hormone (GH) ind
uced craniofacial changes might explain persisting OSA despite endocrine in
activity in acromegaly.
Nineteen patients treated for acromegaly were examined cephalometrically fo
r craniofacial changes and polysomnographically for OSA. Twelve patients pr
oved to have OSA with an apnoea/hypopnoea index >15; seven patients showed
no evidence of OSA at all.
With respect to the endocrinological parameters, there were no differences
between the two groups that would explain the presence or absence of OSA. N
either group differed with respect to sex, age, or body mass index. Craniof
acial changes were predominantly found in the mandible. The group,vith OSA
proved to have increased vertical, dolichofacial growth compared to those w
ithout OSA. Consecutively, in the OSA group the posterior airway space was
narrowed, and the hyoid was displaced more caudally.
Thus, it seems that craniofacial structures of patients,vith acromegaly and
persisting obstructive sleep apnoea are different from those without obstr
uctive sleep apnoea. Surgical corrections of pertaining acromegaly-induced
craniofacial changes should be performed with an awareness of the individua
l craniofacial condition so as not to enhance obstructive sleep apnoea.